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LeGrand and colleagues (1) concluded, on the basis of their recent review of the literature, that furosemide has no role in the modern management of hypercalcemia. We take issue with this contention and note the fundamental limitations of their analysis.

Bisphosphonates attenuate bone calcium mobilization and address a major—but not the sole—clinical contributor to hypercalcemia. Hypercalcemia may also result from increased gastrointestinal calcium uptake. Decreased renal excretion alone does not cause hypercalcemia but does aggravate hypercalcemia from other causes. Volume contraction and dehydration due to natriuresis and nephrogenic diabetes insipidus, respectively, also amplify hypercalcemia of all causes. The calciuretic effect of furosemide and its enhancement by volume expansion, however, are well established: Natriuresis promotes calciuresis.